Typical atrial flutter from blunt cardiac injury: an atypical cause

Naji Maaliki, Fadi Kandah Aleem Azal Ali James Farah, Temitope Akinjogbin,Francesco Franchi

1. Internal Medicine, University of Florida College of Medicine-Jacksonville, Florida, USA; 2. General Surgery, University of Florida College of Medicine-Jacksonville, Florida, USA; 3. Division of Cardiology, University of Florida College of Medicine-Jacksonville, Florida, USA

Atrial flutter (AFL) is a detrimental cardiac arrhythmia caused by multiple pathologic conditions. Certain unsuspecting cases,however, may be an inciting factor. Among them is blunt cardiac injury (BCI), characterized by nonpenetrating mediastinal trauma, leading to arrhythmias due to myocardial tissue injury. AFL is a rare sequela of BCI that has seldom been reported.We present a case of a healthy 50-year-old lady who was incidentally diagnosed with AFL in the setting of BCI.

A 50-year-old lady with a past medical history of hypertension presented after a motor vehicle accident. Driving at roughly 30 miles per hour, she suddenly swerved into a tree to avoid hitting a dog,which resulted in airbag deployment and a transient loss of consciousness. She was hemodynamically stable, anxious, and complained of chest wall tenderness, headache, and palpitations. Physical exam revealed tachypnea, tachycardia with a regular rhythm, soft abdomen, and seatbelt signs on the left neck, left and right breasts, and right upper abdomen. A trauma survey, including a whole-body computed tomography scan, confirmed the absence of significant injury. Surprisingly, she had a regular tachycardia with a rate of 150 beats per minute.Electrocardiogram (ECG) displayed a 2:1 AFL suggestive of typical counterclockwise conduction (Figure 1).Workup with chest imaging, complete blood count,electrolytes, cardiac biomarkers, thyroid-stimulating hormone, and toxicology panel was normal. She did not have any congenital, cardiac, or pulmonary diseases, and her family history was unremarkable.She had only been on extended-release Nifedipine for hypertension and did not take any other medications or recreational drugs. Transthoracic echocardiography demonstrated a normal global systolic function with no structural abnormalities. The patient was started on Metoprolol Tartrate for rate control and Apixaban for a CHA2DS2-VASc of 2.The next day, the patient still had intermittent palpitations and chest wall tenderness without significant distress, but later spontaneously converted back to normal sinus rhythm (Figure 2). The electrophysiology team evaluated her, and she underwent a cavotricuspid isthmus ablation with a bidirectional block. She was discharged home on apixaban in stable conditions with scheduled follow-up.

Typical AFL is a tachyarrhythmia identified by rapid atrial depolarizations from an overactive macroreentrant circuit that traverses the cavotricuspid isthmus. It commonly involves a counterclockwise circuit rotation around the tricuspid valve, contrasted to the rare clockwise direction.[1]Typical counterclockwise AFL is characterized by a regular atrial rate of around 300 beats per minute,seen as sawtooth atrial “F” waves with a negative deflection in the inferior leads and a positive deflection in lead V1, followed by a regular ventricular rate of around 150 beats per minute when there is 2:1 atrioventricular conduction.[2]Symptoms include dyspnea, palpitations, lightheadedness, chest pain, and anxiety. Complications may be syncope,heart failure, myocardial ischemia, and systemic embolism. Diagnosis is mainly through ECG analysis, followed by imaging and laboratory investigations to evaluate for etiology. The optimal treatment is flutter ablation, which has around a 97%success rate of sinus rhythm conversion.[3]If not feasible, pharmacologic rhythm control or rate control with negative chronotropic agents may be used,along with anticoagulation for stroke risk reduction if considered appropriate by the stratification scores(CHA2DS2-VASc & HAS-BLED).

Figure 1 Electrocardiogram on presentation. Initial electrocardiogram demonstrating sawtooth atrial “F” waves at a rate of 300 beats per minute with a positive deflection in V1 and negative deflection II, III, aVF, and a regular tachycardia rate of 150 beats per minute,all of which are indicative of 2:1 atrial flutter.

Figure 2 Electrocardiogram after spontaneous conversion. Electrocardiogram obtained on day 2 admission demonstrating a normal sinus rhythm.

AFL rarely occurs in a normal heart, so it was essential to determine the cause.[4]The workup ruled out electrolyte derangements, thyrotoxicosis, anemia, toxicology, and dehydration. Echocardiography confirmed a structurally normal heart with good function and no chamber or valvular abnormalities. While angiography was not done,ischemia was unlikely due to the absence of ischemic changes on ECG, wall motion abnormalities on echocardiography, nor a history of angina or its equivalents. She denied any prior palpitations or dyspnea and had consistent primary care visits with well-controlled hypertension and no irregularities.

The BCI was deemed as the probable inciting factor for the new-onset AFL. BCI is termed as cardiac damage due to non-penetrating trauma to the heart and is mostly caused by motor vehicle accidents.[5]BCI is associated with multiple arrhythmias,ranging from benign or transient rhythms to lifethreatening dysrhythmias such as ventricular fibrillation. Atrial fibrillation has been the most frequently reported arrhythmia resulting from BCI,with few AFL cases mentioned.[6]The mechanism by which this occurs is multifaceted. Firstly, an intrathoracic bleed must be ruled out as the most likely cause of reflex tachycardia.[7]The blunt trauma may damage the cardiac autorhythmic, conducting cells, or contractile cells leading to conduction aberrancy.[8]Deduced from histologic studies,resultant microhemorrhages, inflammatory infiltrate with subsequent cardiac cell necrosis, and interstitial edema may contribute to cell injury.[9]The inflammation surrounding the vessels and potential intravascular rouleaux formation may also lead to local microvascular cardiac ischemia.[6]Additionally, the trauma force may start a reflex catecholamine surge that can further induce a tachyarrhythmia.[6,8]Previous meta-analyses had postulated that the risk of arrhythmia directly correlates with the force and speed of trauma but is inversely related to the area.[6,7]The severity of arrhythmia also corresponds with the timing of impact in relation to the cardiac cycle, as exemplified by cases of commotio cordis.[10]

In our patient, whether the BCI was solely responsible for the arrhythmia is challenging to determine, as it may have unmasked a silent cardiac disease or tendency to develop one. Nevertheless,this case highlights the importance of ruling out cardiac arrhythmias in patients with BCI who present with tachycardia. Thus, it is reasonable to conduct a more rigorous cardiac workup to evaluate other diseases in those who develop arrhythmia after cardiac trauma.

ACKNOWLEDGMENTS

All authors had no conflicts of interest to disclose.